MCL cel lines upon OMP-52M51 treatment
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE125349 | GEO | 2019/01/19
REPOSITORIES: GEO
Similar Datasets
Project description:MCL cel lines upon OMP-52M51 treatment
| PRJNA515904 | ENA
Project description:We recently demonstrated that a human Notch1-specific neutralizing antibody (OMP-52M51) was very effective in T-ALL patient derived xenografts (PDX) bearing NOTCH1/FBW7 mutations. To evaluate the transcriptomic downstream effects of anti-NOTCH1 therapy, we perform RNA-Seq analysis in leukemia cells derived from PDTALL46 PDX mice after an acute treatment with control Ab or OMP-52M51.
2023-09-13 | GSE224988 | GEO
Project description:Notch signaling is critical for vascular morphogenesis by co-determining the sprouting behavior of endothelial cells. Here, we investigate the function of ubiquitin-specific peptidase 10 (USP10) in regulation of the turnover of the NOTCH1 intracellular domain. HUVEC were transfected with scrambled or USP10 targeting siRNA and then stimulated by treatment with DLL4 or control. RNA for analysis was isolated after 24 hours of DLL4 stimulation.
2019-04-26 | E-MTAB-7774 | biostudies-arrayexpress
Project description:OMP is expressed only in mature olfactory sensory neurons, arguing that its function is specially suited to the needs of OSNs. However none of the properties of OMP suggest any direct role in regulating gene expression in OSNs. Our data confirms that gene expression in the olfactory epithelium of mice lacking OMP is indistinguishable from mice expressing OMP. We used affymerix M430v2.0 gene chips to cover as much of genome as possible and observed no statistically significant differences in mRNA abundance between the two genotypes.These results imply that OMPs ability to regulate signal transduction with in OSNs has little effect on gene expression and that its ability to promote mitosis in neighbouring cells (under culture conditions) is insufficiently active under normal laboratory housing conditions to generate detectable differences in gene expression patterns. Keywords: genetic modification
2007-04-30 | GSE4927 | GEO
Project description:Dll4-Notch signaling is required for cell fate decisions and neoplasias. However, emerging evidence suggests a role for Dll4-Notch signaling in metabolic and immune diseases. To date, there is no evidence of a direct effect of Dll4-Notch signaling inhibition on pancreatic islet function and insulin secretion.
2018-08-13 | PXD005333 | Pride
Project description:The Notch pathway is a major regulator of endothelial transcriptional specification. Targeting the Notch receptors or the ligand Dll4 dysregulates angiogenesis. Here, by analyzing single and compound genetic mutants for all Notch signaling members, we find significant differences in the way ligands and receptors regulate liver vascular homeostasis. Loss of Notch receptors caused endothelial hypermitogenic cell-cycle arrest and senescence. Conversely, Dll4 loss triggered a strong Myc-driven transcriptional switch, inducing endothelial proliferation and the tip-cell state. Myc loss suppressed the induction of angiogenesis in the absence of Dll4, without preventing the vascular enlargement and organ pathology. Similarly, inhibition of other pro-angiogenic pathways, including MAPK/ERK and mTor, had no effect on the vascular expansion induced by Dll4 loss; however, anti-VEGFA treatment prevented it without fully suppressing the transcriptional and metabolic programs. This study shows incongruence between single-cell transcriptional states, vascular phenotypes, and related pathophysiology. Our findings also suggest that vascular structure abnormalization, rather than neoplasms, causes the reported anti-Dll4 antibody toxicity.
2023-05-12 | GSE231612 | GEO
Project description:OMP is expressed only in mature olfactory sensory neurons, arguing that its function is specially suited to the needs of OSNs. However none of the properties of OMP suggest any direct role in regulating gene expression in OSNs. Our data confirms that gene expression in the olfactory epithelium of mice lacking OMP is indistinguishable from mice expressing OMP. We used affymerix M430v2.0 gene chips to cover as much of genome as possible and observed no statistically significant differences in mRNA abundance between the two genotypes.These results imply that OMPs ability to regulate signal transduction with in OSNs has little effect on gene expression and that its ability to promote mitosis in neighbouring cells (under culture conditions) is insufficiently active under normal laboratory housing conditions to generate detectable differences in gene expression patterns. Experiment Overall Design: The overall design of the experiment is to undertand the effect of OMP (olfactory marker protein) on gene expression in the olfactory epithelium. We isolated the olfactory epithelium from homozygous and heterozygous OMP-GFP mice, extracted the RNA and hybridized on to the mouse expression set 430 2.0 Chip.
2008-06-13 | E-GEOD-4927 | biostudies-arrayexpress
Project description:The Notch pathway is a major regulator of endothelial transcriptional specification. Targeting the Notch receptors or the ligand Dll4 induces angiogenesis. Here, by analyzing single and compound genetic mutants for all Notch signaling members, we find significant differences in the way ligands and receptors regulate liver vascular homeostasis. Loss of Notch receptors caused endothelial hypermitogenic cell-cycle arrest and senescence. Conversely, Dll4 loss triggered a strong Myc-driven transcriptional switch inducing endothelial proliferation and the tip-cell state. Myc loss suppressed the induction of angiogenesis in the absence of Dll4, without preventing the vascular enlargement and organ pathology. Similarly, inhibition of other pro-angiogenic pathways, including MAPK/ERK and mTor, had no effect on the vascular expansion induced by Dll4 loss, however, anti-VEGFA treatment prevented it without fully suppressing the transcriptional and metabolic programs. This study shows incongruence between single-cell transcriptional states, vascular phenotypes, and related pathophysiology. Our findings also suggest that the vascular structure abnormalization, rather than neoplasms, causes the reported anti-Dll4 antibody toxicity.
2023-05-12 | GSE229793 | GEO
Project description:Coronaries are essential for myocardial growth and heart function. Notch is crucial for mouse embryonic angiogenesis, but its role in coronary development remains uncertain. We show Jag1, Dll4 and activated Notch1 receptor expression in sinus venosus (SV) endocardium. Endocardial Jag1 removal blocks SV capillary sprouting, while Dll4 inactivation stimulates excessive capillary growth, suggesting that ligand antagonism regulates coronary primary plexus formation. Later endothelial ligand removal, or forced expression of Dll4 or the glycosyltransferase MFng, blocks coronary plexus remodeling, arterial differentiation, and perivascular cell maturation. Endocardial deletion of Efnb2 phenocopies the coronary arterial defects of Notch mutants. Angiogenic rescue experiments in ventricular explants, or in primary human endothelial cells, indicate that EphrinB2 is a critical effector of antagonistic Dll4 and Jag1 functions in arterial morphogenesis. Thus, coronary arterial precursors are specified in the SV prior to primary coronary plexus formation and subsequent arterial differentiation depends on a Dll4-Jag1-EphrinB2 signaling cascade.
2019-12-03 | GSE110614 | GEO
Project description:The purpose of this study is to test the safety and efficacy of an experimental drug, OMP-305B83, when given in combination with FOLFIRI or FOLFOX. OMP-305B83 is a humanized bispecific monoclonal antibody and was developed to target cancer stem cells. Based on preclinical studies, it is believed that OMP-305B83 may block the growth of cancer stem cells and may also impair the productive growth of new blood vessels, which tumors need to grow and spread.
The study is sponsored by OncoMed Pharmaceuticals, which is referred to as OncoMed or the Sponsor.
| 2235323 | ecrin-mdr-crc